Influence of Ethanol and Microsomal Drugs on Hepatic Hemodynamics*

Leevy, Carroll M.; tenHove, Willem; Opper, Anita; Popovic, Stanislav

doi:10.1111/j.1749-6632.1970.tb37023.x

Cited by 21 publications

(2 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Haemodynamic disturbances in cirrhosis, such as intra-and extrahepatic shunts, diminish the effective sinusoidal blood flow (Popper et al, 1952, Groszmann et al, 1972Groszmann et al, 1977). It is also evident that in parenchymal liver diseases, such as fatty liver or alcoholic hepatitis, the architectural distortion secondary to infiltration of fat and inflammatory cells, ballooning of the hepatocytes, liver cell hyperplasia, tissue necrosis and active regeneration, may interfere with the sinusoidal perfusion (Leevy, ten Hove, Opper & Popovic 1970, Preisig, Bircher & Paumgartner, 1972. When part of the hepatocytic mass, otherwise with normal or slightly decreased function, is shut off from the effective hepatic perfusion, the reasonable consequence is diminished drug clearance.…”

Section: Discussionmentioning

confidence: 99%

Roles of hepatic blood flow and enzyme activity in the kinetics of propranolol and sotalol.

Pirttiaho¹,

Ea²,

Pelkonen³

et al. 1980

Brit J Clinical Pharma

View full text Add to dashboard Cite

1 The roles of the hepatic blood flow and the drug oxidizing enzyme system in eliminating oral propranolol and sotalol were studied in twelve subjects with biopsy proven liver parenchymal disease. 2 The apparent plasma clearance of propranolol was closely related both to the in vivo (antipyrine test) and in vitro (cytochrome P450) indices of the activity of the hepatic mixed function oxidase system.3 Propranolol clearance had also a clear relationship to the estimated liver blood flow. Altered flow was, however, suggested to be a minor factor when compared with changes in the enzyme system. 4 The elimination rate of sotalol had no correlation to the indices of hepatic drug metabolism or to the estimated liver blood flow. 5 It is concluded that both the deteriorated sinusoidal perfusion and the decreased mass of drug metabolizing enzymes may be responsible for the impaired elimination of oral propranolol in subjects with parenchymal liver disease.

show abstract

Section: Discussionmentioning

confidence: 99%

Roles of hepatic blood flow and enzyme activity in the kinetics of propranolol and sotalol.

Pirttiaho¹,

Ea²,

Pelkonen³

et al. 1980

Brit J Clinical Pharma

View full text Add to dashboard Cite

show abstract

“…6 An alternative experimental model of hepatocyte enlargement that has received little attention is chronic phenobarbitone ingestion. Phenobarbitone has been reported to induce an increase in hepatocyte volume of over 90% 12 ; prolonged phenobarbitone treatment is capable of inducing clinicallysignificant portal hypertension, 13 which has been classified as an intrahepatic sinusoidal cause of portal hypertension, 14 although the mechanisms involved have not been fully investigated.…”

mentioning

confidence: 99%